<p>Pinocembrin Ameliorates Cognitive Impairment Induced by Vascular Dementia: Contribution of Reelin-dab1 Signaling Pathway</p>

Abstract

Background: As a substrate of apoER2, Reelin has been verified to exert neuroprotection by preventing memory impairment. Pinocembrin is the most abundant natural flavonoid found in propolis, and it has been used to exert neuroprotection, blood-brain barrier protection, anti-oxidation, and inflammation diminishing, both in vitro and in vivo. However, the roles and molecular mechanisms of pinocembrin in neurobehavioral outcomes and neuronal repair after vascular dementia are still under investigation. Purpose: To explore the role of pinocembrin in the involvement of the Reelin-dab1 signaling pathway in improving memory impairment, both in cell culture and animals experiments. Material and Methods: Behavioral tests were conducted on day 48 to confirm the protection of pinocembrin against cognitive impairment. Cell and molecular biology experiments demonstrated that the Reelin-dab1 pathway mediates the underlying mechanism of cognitive improvement by pinocembrin. Results: It was showed that pinocembrin alleviated learning and memory deficits induced by vascular dementia, by inducing the expression of Reelin, apoER2, and p-dab1 in the hippocampus. The expression of Reelin and p-dab1 was both inhibited following Reelin RNA interference in SH-SY5Y prior to oxygen glucose deprivation (OGD) injury, suggesting that Reelin played a core role in pinocembrin's effect on OGD in vitro. Conclusion: Pinocembrin improves the cognition via the Reelin-dab1 signaling pathway.

Brain Factor-7® Improves Cognitive Impairment Following Transient Ischemia and Reperfusion Injury in Gerbil Forebrain through Promoting Remyelination and Restoring Cholinergic and Glutamatergic Neurotransmission in the Hippocampus

“…Previous studies on materials possessing beneficial properties against ischemia and reperfusion injury-induced cognitive dysfunction have shown that behavioral improvement including learning and spatial memory functions in rodent models of ischemic stroke is accomplished [2,4,34,35]. For example, Yan et al [35] have reported that treatment with dimethyl fumarate (an FDA-approved therapeutic for multiple sclerosis) to rats with chronic cerebral hypoperfusion injury can improve cognitive impairment possibly via alleviating oxidative stress damage and neuroinflammation, and inhibiting ferroptosis of neurons in the hippocampus.…”

Metabolic Syndrome and Vascular-Associated Cognitive Impairment: a Focus on Preclinical Investigations

“…The Chinese herb mix Chitosan reduces hippocampal-memory impairment and reduces neuron cell loss induced by CCAO while also significantly reversing reactive oxygen species production, neuronal apoptosis and microglia overactivation in the hippocampus through activation of the antioxidative response element Nrf2 (NF-E2 p45-related factor 2) causing the subsequent upregulation in the expression of many cytoprotective enzymes [ 72 ]. Meanwhile, Pinocembrin, a flavonoid with antioxidant properties [ 73 ] alleviated learning and memory deficits induced by CCAO and attenuated hippocampal neuronal damage by inducing the upregulation of the Reelin-Dab1 signalling pathway in the hippocampus [ 74 ], previously reported to exert a key role in the adult brain by promoting learning and memory [ 75 ]. Moreover in a dietary MetSyn-VCI model, gallic acid, a polyphenol and antioxidant present in grapes and green tea [ 76 ] improved recognition memory and increased hippocampal dendritic spine numbers by reducing the oxidative and inflammatory environment [ 77 ].…”